• Loss of deep tendon reflexes in lower limbs
• Loss of joint positions sense and vibration (doral columns) and stamping gait. (tabetic gait)
• Urinary retention

    - there is a peculiar pattern of reflex preservation: 
        - **Loss of reflexes (lower motor sing) with up-going Babinski reflex. (upper motor sign)**

1. Promyelocytic variant - there is thrombocytopenia and DIC -> leading to a bleeding tendency. -> This variant is a medical emergency; high rate of early mortality. Complications: pulmonary or cerebral haemorrhage.
2. Some variant causing Gingival hyperplasia - monocytic subtypes M4 and M5
   1. 

[!TIP] Mnemonic: Seeing gum hyperplasia should make you PANiC
Panic if you see gum hyperplasia

• Phenytoin
• AML <- "rapidly forming gingival hyperplasia is usually the first sign of this disease" Source
• Nifedipine
• Ciclosporin

Treatment of AML

Current standard chemotherapy regimens cure only a minority of patients with AML.
Source
Most young patients should be considered for allogenic stem cell transplantation.

Note: Dead space is NOT a cause for hypoxaemia
: DH-DLS

| purpura - | purpura + (with normal PLT count) | purpura - | purpura of lower extremities |

• joint involvement can be monoarticular, oligoarticular (upto 4) and polyarticular (≥5).

• Z line deformity

  • Commonly affected; causes functional impairment, especially after rotator cuff tears (which occur in RA).
  • Being a more proximal joint, it's affected later on in the disease.

• Constitutional:

  • Generalized aches and stiffness, weight loss, depression, fatigue

• Skin

  • about 40% of rheumatoid nodules.
  • Subcutaneous nodules which may or may not be attached to underlying joint capsules / tendons.
  • Generally on sites of repeated stress / pressure. Commonest site is elbows; Occiput and sacrum of bed ridden patients.
  • Normally, only of cosmetic concern unless on functional areas like the sole of the foot.

• Hands

  • Bilateral Carpal tunnel syndrome
  • Tendon nodules which can cause
    • Tendon rupture (esp. of extensor pollicis longus)
    • Trigger finger
    • tenosynovitis -> Decreased grip strength and range of motion. [[tendonSheathAnatomy.png]]

• Rheumatoid lung disease: mnemonic: affects all parts of the lungs

  • Pleura - pleuritis - the commmonest pulmonary manifestation -> pleuritic chest pain.

• Cardiac: pericarditis is the commonest.

  • Mitral regurgitation is an association.

• Sjogren syndrome: this is defined as presence of xerostomia or keratoconjuntivitis sicca in the presence of another connective tissue disease.

• haematological:

  • Anaemia** is universal: Normochromic, normocytic.
  • Thrombocytosis: with active disease
  • Felty's syndrome: The triad of neutropenia, splenomegaly and nodular RA
  • Also associated with lymphoma

Cauda equina is composed for 18 nerve roots. 2 or more are involved -> called cauda equina syndrome.

[!INFO] Compare with Conus medullaris syndrome:

• Conus medullaris: sudden onset, upper and lower motor symptoms present.
• knee jerk is preserved.
• less severe radicular pain.
• peri anal numbness ?not a dermatomal distribution
• impotence is more common than in cauda equina
• cauda equina can cause overflow incontinence in late stages but conus medullaris causes these in early diseases

Infective aetiologies of cauda equina

• lyme disease
• TB
• and others.

Features of cauda equina syndrome

Cardiac biomarkers

[!INFO] Types of biomarkers

Don't confuse the different types of biomarkers used in MI.

[!INFO] Key points for exams:

• myoglobin is the first to rise
• CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days (troponin T remains elevated for up to 10 days)
• 
• Troponin levels rise within two to three hours of the onset of chest pain Source

The skeletal and cardiac isoforms of TnT (troponin T) and TnI (troponin I) are distinct. <- that's what's measured in MI.

cTnT = "cardiac troponin T"
skTnI = "skeletal troponin I"

Data suggest that brief periods of ischemia, sudden increases in preload, and physiological challenges like tachycardia and catecholamines can lead to the release of cTn.
4. Pulmonary embolism / pulmonary disease <- caused by right heart strain

Creatine kinase

• CK-MM, found in your skeletal muscle and heart.
• CK-MB, found in the heart and rises when heart muscle is damaged.
• CK-BB, found mostly in your brain. It's also found in smooth muscles such as the intestine or uterus.

• Palpable purpura (non thrombocytopaenic purpura) -> no thrombocytopaenia.

Alpha-1 antitrypsin deficiency

• Is a protease inhibitor which protects tissues against the action of enzymes like neutrophil elastase.
• Deficiency causes emphysema.
• INheritance: #autosomal-Recessive
• Genetic variants:
  • PiMM = normal individual
  • PiMZ = heterozygous; risk of emphysema developing if patient is a smoker.
  • PiSS = 50% of normal antitrypsin levels;
  • PiZZ = 10% of antitrypsin levels; affected and develops emphysema

Management: intravenous alpha1-antitrypsin protein concentrates + smoking cessation, supportive bronchodilators etc .

Source <- Dynamic air trapping in COPD.